Abstract. We formulate and analyze a simple dynamical systems model for climate-vegetation interaction. The planet we consider consists of a large ocean and a land surface on which vegetation can grow. The temperature affects vegetation growth on land and the amount of sea ice on the ocean. Conversely, vegetation and sea ice change the albedo of the planet, which in turn changes its energy balance and hence the temperature evolution. Our highly idealized, conceptual model is governed by two nonlinear, coupled ordinary differential equations, one for global temperature, the other for vegetation cover. The model exhibits either bistability between a vegetated and a desert state or oscillatory behavior. The oscillations arise through a Hopf bifurcation off the vegetated state, when the death rate of vegetation is low enough. These oscillations are anharmonic and exhibit a sawtooth shape that is characteristic of relaxation oscillations, as well as suggestive of the sharp deglaciations of the Quaternary.Our model's behavior can be compared, on the one hand, with the bistability of even simpler, Daisyworld-style climate-vegetation models. On the other hand, it can be integrated into the hierarchy of models trying to simulate and explain oscillatory behavior in the climate system. Rigorous mathematical results are obtained that link the nature of the feedbacks with the nature and the stability of the solutions. The relevance of model results to climate variability on various timescales is discussed.

Time delays are known to play a crucial role in generating biological oscillations. The early embryonic cell cycle in the frog Xenopus laevis is one such example. Although various mathematical models of this oscillating system exist, it is not clear how to best model the required time delay. Here, we study a simple cell cycle model that produces oscillations due to the presence of an ultrasensitive, time-delayed negative feedback loop. We implement the time delay in three qualitatively different ways, using a fixed time delay, a distribution of time delays, and a delay that is state-dependent. We analyze the dynamics in all cases, and we use experimental observations to interpret our results and put constraints on unknown parameters. In doing so, we find that different implementations of the time delay can have a large impact on the resulting oscillations.

In an oscillatory medium, a region which oscillates faster than its surroundings can act as a source of outgoing waves. Such pacemaker-generated waves can synchronize the whole medium and are present in many physical and biological systems, where they are a means of transmitting information. Through numerical simulations, we quantify how the properties of the pacemaker and the underlying limit cycle determine the wave speed, as well as the speed with which they overtake the medium. We compare oscillators based on two of the main mechanisms that generate oscillations in biochemical systems: bistability and time delay. We show that these mechanisms produce oscillations whose wave propagation properties differ markedly. While both types of oscillatory media admit waves that propagate linearly outwards, the dependence of the wave speed on a timescale separation parameter is different between the two. If timescale separation is lost, waves no longer spread linearly. Finally, we quantify the effects of pacemaker size, the frequency difference with the surroundings, and the diffusion strength.

Bistability is a common mechanism to ensure robust and irreversible cell cycle transitions. Whenever biological parameters or external conditions change such that a threshold is crossed, the system abruptly switches between different cell cycle states. Experimental studies have uncovered mechanisms that can make the shape of the bistable response curve change dynamically in time. Here, we show how such a dynamically changing bistable switch can provide a cell with better control over the timing of cell cycle transitions. Moreover, cell cycle oscillations built on bistable switches are more robust when the bistability is modulated in time. Our results are not specific to cell cycle models and may apply to other bistable systems in which the bistable response curve is time-dependent.